New research into the causes of chronic pain may lead to more effective medical diagnoses and treatment, according to U of T physiology professor Michael Salter.
In a field that one specialist describes as “one of the most exciting areas in medicine,” Salter has made significant discoveries about how the body’s pain system functions and what goes amiss to cause chronic pain. For according to the Chronic Pain Association of Canada, this afflicts 18 per cent of Canadians.
Unlike normal acute pain-which warns us about actual or potential harm to the body-chronic pain has no known defensive or helpful functions. According to a recent scientific review, chronic pain can be “intense, unremitting and often resistant to all currently available therapies.”
It may result from damage to the central or peripheral nervous system, due to surgery, bone compression in cancer, or other medical conditions. But until recently, its basic mechanisms have been poorly understood.
A medical doctor by training, Salter has been doing research at U of T since 1978. In 2000, he helped found Salter, the U of T centre for the study of pain (UTCSP), which he leads.
In 2002, in a paper in the journal Cell, he identified a a so-called “pain gene.” He showed that the absence of a gene called DREAM reduced the sensitivity of mice to pain.
For the understanding he has brought to the mechanisms of pain, Salter was elected as a Fellow of the Royal Society of Canada this year.
Much of his research has focused on the cellular and molecular means that transmit pain signals between the neurons of the dorsal horn (a part of the spinal cord that processes these signals).
According to Salter, a key characteristic of the body’s pain system is neuronal plasticity-the capacity of neurons to change their function, chemical profile, or structure. For neurons do more than simply relay pain signals through the nervous system to the brain; they can themselves be altered in the transmission process.
Changes in how the neurons function can become pathological, causing pain hypersensitivity.
“Previously it was thought that the nervous system was a passive recipient of information. We now know that that’s a very antiquated view,” said Salter.
One of the major discoveries by Salter and his team is that cells called glia (from the Greek word for glue) play an active role in pain processes following nerve injury. Originally thought to serve primarily housekeeping functions, glia become active following nerve injuries and appear to play an important role in helping neurons transmit pain signals. However, the precise mechanisms that cause glia to affect neurons in this way remain unclear.
Researchers hope that a better understanding of the pain system will lead to new drugs that can target specific pain mechanisms or processes.
“There are lots of ideas out there. The big question is which ones are going to have a potential for working,” Salter said.
He also noted that better diagnoses may help dispel misconceptions about the nature of pain, as well as the stigma that can attach to chronic pain sufferers.
“The paradox is that you can look totally normal but have severe pain.”
